Inflammation and insulin resistance

de Luca, Carl; Olefsky, Jerrold M.

doi:10.1016/j.febslet.2007.11.057

Cited by 1,161Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismCardiovascular Disease and Adiposity

Inflammation and insulin resistance

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de Luca, Carl, Olefsky, Jerrold M.·2008·FEBS Letters

DOI 10.1016/j.febslet.2007.11.057PMC PMC2246086

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Abstract

Obesity‐induced chronic inflammation is a key component in the pathogenesis of insulin resistance and the Metabolic syndrome. In this review, we focus on the interconnection between obesity, inflammation and insulin resistance. Pro‐inflammatory cytokines can cause insulin resistance in adipose tissue, skeletal muscle and liver by inhibiting insulin signal transduction. The sources of cytokines in insulin resistant states are the insulin target tissue themselves, primarily fat and liver, but to a larger extent the activated tissue resident macrophages. While the initiating factors of this inflammatory response remain to be fully determined, chronic inflammation in these tissues could cause localized insulin resistance via autocrine/paracrine cytokine signaling and systemic insulin resistance via endocrine cytokine signaling all of which contribute to the abnormal metabolic state.

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Evidence indicates that inflammation causes insulin resistance.
“Evidence indicates that inflammation causes insulin resistance”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [281]
Intake of flavonols and flavones was not correlated with plasma CRP or IL-6 concentrations in healthy women with BMI 25.8-26.2 kg/m2.
“The intake of flavonols and flavones was not correlated with plasma concentrations of CRP or IL-6 in healthy women (BMI 25•8-26•2 kg/m 2 ) (801) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [801]
Several cytokines and chemokines, including CCL2, IL-6, IL-1β, MIF, and TNF-α, can be released by adipocytes and macrophages.
“Several cytokines and chemokines, such as CCL2, IL-6, IL-1β, macrophage migration inhibitory factor (MIF), and TNF-α, can be released by adipocytes and macrophages (83)(84)(85).”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [83]
Adipocytes are the unique source of secreted adipokines such as leptin and adiponectin, which can promote insulin sensitivity, and resistin and retinol-binding protein 4, which can impair insulin sensitivity.
“Adipocytes are the unique source of secreted adipokines such as leptin and adiponectin, which can promote insulin sensitivity, as well as resistin and retinol-binding protein 4 (RBP4), which can impair insulin sensitivity (83)(84)(85).”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [83]
Elevated levels of TNF-α, IL-6, and C-reactive protein have been shown in individuals with insulin resistance and diabetes.
“Consistent with this, elevated levels of the proinflammatory cytokines TNF-α, IL-6, and C-reactive protein (CRP) have been shown in individuals with insulin resistance and diabetes (for review, see refs.[83][84][85].”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [83]

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Authors: de Luca, C., & Olefsky, J. M.
Affiliations: University of California San Diego (US)
Corresponding author: Olefsky, Jerrold M.
ORCID: Olefsky, Jerrold M.
Venue: FEBS Letters
Publisher: Wiley
Published: 2007-11-29
Volume: 582
Issue: 1
Pages: 97-105
ISSN: 0014-5793 (ISSN-L)
1873-3468
DOI: 10.1016/j.febslet.2007.11.057
PMC: PMC2246086
OpenAlex: W2031882974
Cited by: 1,161
References: 66
Citations by year: 2026: 56 · 2025: 68 · 2024: 54 · 2023: 83 · 2022: 82 · 2021: 83 · 2020: 68 · 2019: 64 · 2018: 73 · 2017: 69 · 2016: 58 · 2015: 56 · 2014: 40 · 2013: 65 · 2012: 58
FWCI: 5.45
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: FEBS Letters (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases (DK 074868, DK 033651, T32DK007494, R37DK033651, DK007494, P01DK074868)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (U54HD012303)
Topics: Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords: insulin resistance, obesity, chronic inflammation, metabolic syndrome, inflammatory cytokines, adipose tissue, skeletal muscle, liver, insulin signaling, macrophages, autocrine and paracrine signaling
MeSH terms: Humans, Inflammation, Insulin Resistance, Signal Transduction

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Inflammation and insulin resistance

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